Evidence map›Paper›PMID 26549310›Full record

ArticleScientific reports2015

Reciprocal regulation of RORγt acetylation and function by p300 and HDAC1.

Qingsi Wu, Jia Nie, Yayi Gao, Peng Xu, Qijuan Sun, Jing Yang, Lei Han, Zuojia Chen, Xiuwen Wang, Ling Lv and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  16. Epigenetic Reprogramming of CD4Frontiers in immunology · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 1 country.

Qingsi WuDepartment of Immunology, Anhui Medical University, Hefei, Anhui, 230032, China.
Jia NieKey Laboratory of Molecular Virology &Immunology, Unit of Molecular Immunology, Institute Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Yayi GaoKey Laboratory of Molecular Virology &Immunology, Unit of Molecular Immunology, Institute Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Peng XuDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230032, China.
Qijuan SunDepartment of Microbiology and Parasitology, Anhui Medical University, Hefei, Anhui, 230032, China.
Jing YangKey Laboratory of Molecular Virology &Immunology, Unit of Molecular Immunology, Institute Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Lei HanDivision of Rheumatology, Huashan Hospital, Fudan University, Shanghai 200040, China.
Zuojia ChenKey Laboratory of Molecular Virology &Immunology, Unit of Molecular Immunology, Institute Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Xiuwen WangDivision of Rheumatology, Huashan Hospital, Fudan University, Shanghai 200040, China.
Ling LvDivision of Rheumatology, Huashan Hospital, Fudan University, Shanghai 200040, China.
Andy TsunKey Laboratory of Molecular Virology &Immunology, Unit of Molecular Immunology, Institute Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Jijia ShenDepartment of Immunology, Anhui Medical University, Hefei, Anhui, 230032, China.
Bin LiKey Laboratory of Molecular Virology &Immunology, Unit of Molecular Immunology, Institute Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Institut Pasteur of Shanghai · CNAnhui Medical University · CNFudan University · CNHuashan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T helper 17 (Th17) cells not only play critical roles in protecting against bacterial and fungal infections but are also involved in the pathogenesis of autoimmune diseases. The retinoic acid-related orphan receptor (RORγt) is a key transcription factor involved in Th17 cell differentiation through direct transcriptional activation of interleukin 17(A) (IL-17). How RORγt itself is regulated remains unclear. Here, we report that p300, which has histone acetyltransferase (HAT) activity, interacts with and acetylates RORγt at its K81 residue. Knockdown of p300 downregulates RORγt protein and RORγt-mediated gene expression in Th17 cells. In addition, p300 can promote RORγt-mediated transcriptional activation. Interestingly, the histone deacetylase (HDAC) HDAC1 can also interact with RORγt and reduce its acetylation level. In summary, our data reveal previously unappreciated posttranslational regulation of RORγt, uncovering the underlying mechanism by which the histone acetyltransferase p300 and the histone deacetylase HDAC1 reciprocally regulate the RORγt-mediated transcriptional activation of IL-17.

Indexed as

AcetylationE1A-Associated p300 ProteinGene Expression RegulationHistone Deacetylase 1Histone Deacetylase InhibitorsHumansInterleukin-17Nuclear Receptor Subfamily 1, Group F, Member 3Protein BindingProtein StabilityTh17 CellsTranscription, GeneticE1A-Associated p300 ProteinHistone Deacetylase 1Histone Deacetylase InhibitorsInterleukin-17Nuclear Receptor Subfamily 1, Group F, Member 3

Identifiers

PMID26549310
PMCPMC4817527
OpenAlexW2411886515

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.